Bioessays

Gurevich, Vsevolod V.

doi: 10.1002/bies.202300085pmid: 37246243

Gautron, Laurent

doi: 10.1002/bies.202300056pmid: 37264690

Immunohistochemistry is a commonly used technique in research and pathology laboratories worldwide. However, in recent years, there has been a significant decrease in the number of Pubmed entries using the term immunohistochemistry. This decline can be attributed to two factors: increased awareness of the issue of unreliable research antibodies and the availability of novel RNA in situ hybridization techniques. Using the example of immunohistochemistry, this text discusses the factors that can affect good laboratory and publishing practices, or their lack thereof.

doi: 10.1002/bies.202370071pmid: N/A

Stuehr, Dennis J.; Biswas, Pranjal; Dai, Yue; Ghosh, Arnab; Islam, Sidra; Jayaram, Dhanya Thamaraparambil

doi: 10.1002/bies.202300055pmid: 37276366

A natural heme deficiency that exists in cells outside of the circulation broadly compromises the heme contents and functions of heme proteins in cells and tissues. Recently, we found that the signaling molecule, nitric oxide (NO), can trigger or repress the deployment of intracellular heme in a concentration‐dependent hormetic manner. This uncovers a new role for NO and sets the stage for it to shape numerous biological processes by controlling heme deployment and consequent heme protein functions in biology.

Hsu, Bryan B.

doi: 10.1002/bies.202300096pmid: 37318303

doi: 10.1002/bies.202370072pmid: N/A

Mei, Jie; Huang, Xinyi; Fan, Changyuan; Fang, Jianwu; Jiu, Yaming

doi: 10.1002/bies.202200225pmid: 37254735

During immune responses against invading pathogenic bacteria, the cytoskeleton network enables macrophages to implement multiple essential functions. To protect the host from infection, macrophages initially polarize to adopt different phenotypes in response to distinct signals from the microenvironment. The extracellular stimulus regulates the rearrangement of the cytoskeleton, thereby altering the morphology and migratory properties of macrophages. Subsequently, macrophages degrade the extracellular matrix (ECM) and migrate toward the sites of infection to directly contact invading pathogens, during which the involvement of cytoskeleton‐based structures such as podosomes and lamellipodia is indispensable. Ultimately, macrophages execute the function of phagocytosis to engulf and eliminate the invading pathogens. Phagocytosis is a complex process that requires the cooperation of cytoskeleton‐enriched super‐structures, such as filopodia, lamellipodia, and phagocytic cup. This review presents an overview of cytoskeletal regulations in macrophage polarization, ECM degradation, migration, and phagocytosis, highlighting the pivotal role of the cytoskeleton in host defense against infection.

Frazão, Nelson; Gordo, Isabel

doi: 10.1002/bies.202300063pmid: 37353919

How much bacterial evolution occurs in our intestines and which factors control it are currently burning questions. The formation of new ecotypes, some of which capable of coexisting for long periods of time, is highly likely in our guts. Horizontal gene transfer driven by temperate phages that can perform lysogeny is also widespread in mammalian intestines. Yet, the roles of mutation and especially lysogeny as key drivers of gut bacterial adaptation remain poorly understood. The mammalian gut contains hundreds of bacterial species, each with many strains and ecotypes, whose abundance varies along the lifetime of a host. A continuous high input of mutations and horizontal gene transfer events mediated by temperate phages drives that diversity. Future experiments to study the interaction between mutations that cause adaptation in microbiomes and lysogenic events with different costs and benefits will be key to understand the dynamic microbiomes of mammals. Also see the video abstract here: https://youtu.be/Zjqsiyb5Pk0

Ray, Suhita; Hewitt, Kyle

doi: 10.1002/bies.202300022pmid: 37318311

With decades of research seeking to generalize sterile alpha motif (SAM) biology, many outstanding questions remain regarding this multi‐tool protein module. Recent data from structural and molecular/cell biology has begun to reveal new SAM modes of action in cell signaling cascades and biomolecular condensation. SAM‐dependent mechanisms underlie blood‐related (hematologic) diseases, including myelodysplastic syndromes and leukemias, prompting our focus on hematopoiesis for this review. With the increasing coverage of SAM‐dependent interactomes, a hypothesis emerges that SAM interaction partners and binding affinities work to fine tune cell signaling cascades in developmental and disease contexts, including hematopoiesis and hematologic disease. This review discusses what is known and remains unknown about the standard mechanisms and neoplastic properties of SAM domains and what the future might hold for developing SAM‐targeted therapies.

Cario, Alisa; Berger, Christopher L.

doi: 10.1002/bies.202200138pmid: 37489532

The etiology of Tauopathies, a diverse class of neurodegenerative diseases associated with the Microtubule Associated Protein (MAP) Tau, is usually described by a common mechanism in which Tau dysfunction results in the loss of axonal microtubule stability. Here, we reexamine and build upon the canonical disease model to encompass other Tau functions. In addition to regulating microtubule dynamics, Tau acts as a modulator of motor proteins, a signaling hub, and a scaffolding protein. This diverse array of functions is related to the dynamic nature of Tau isoform expression, post‐translational modification (PTM), and conformational flexibility. Thus, there is no single mechanism that can describe Tau dysfunction. The effects of specific pathogenic mutations or aberrant PTMs need to be examined on all of the various functions of Tau in order to understand the unique etiology of each disease state.